Blood pressure

High blood pressure is an important risk factor for cardiovascular disease, contributing to about 50% of cardiovascular events worldwide and 37% of cardiovascular-related deaths in Western populations. In Australia around 33% of adults over 20 years of age have hypertension and is defined as having a blood pressure reading of above a safe threshold; what is being measured is the pressure of the circulating blood upon the walls of blood vessels. Commonly this threshold is referred to as a systolic (maximum) blood pressure of 140mm Hg and a diastolic blood pressure of 90mm Hg (minimum). Hypertension itself is not a disease but a condition or an indicator of increased risk of cardiovascular disease including coronary heart disease, myocardial infarction (heart attack) or stroke.

Perhaps the best way to look at blood pressure and the plaque in the arteries (atherosclerosis) is through water hydraulics or, even better, the water hose in your garden. The three main components of our vascular system we are concerned with are the pump (heart), pipes (arteries) and feedback valve (kidneys). In your garden there are a few major reasons why the pressure in your water pump increases. If there is not enough water in the pump and pipes or, related to this, the water is too thick. Or the pipes are blocked or too rigid. In your arteries, if you have not consumed enough good clean alkaline mineralised water you literally do not have enough liquid in your heart, arteries and veins to get around the body. It becomes thicker and is too viscous and takes a lot more pressure to get around the body. The kidneys at the other end of the body need to maintain a certain pressure to be able to filter everything through them so they work to regulate the pressure. If the pressure is too low at the kidneys, other problems occur so the kidneys send a message to your heart to increase the pressure, even though this puts added pressure on the heart. In addition, the brain is a unique organ in that it cannot produce its own antioxidants like other tissues in the body can, and when the nutrients including antioxidants, oxygen and glucose it requires get low, it literally shuts down the function so that no damage occurs. As a result the brain also requires a constant flow of blood and if anything slows the flow of blood and nutrients it sends messages to increase the blood pressure. So high blood pressure, while it increases your risk of heart attack, is an essential function of the body to keep functioning as well as it can—not just your body gone wrong. Better to fix the things causing the high blood pressure than to just try to lower it.

Blood that’s too thick also slows the transport of essential nutrients, including oxygen, throughout your body. To help overcome this, drink more water (purified and re-mineralised). It is no coincidence that studies of tea drinkers around the world show those who consume more cups have lower levels of heart attack and stroke. It is not just antioxidants in the tea but also the large volume of liquids they drink.

Secondly, if the pipes in the garden are damaged in some way through oxidative damage from the sun, or if leaks or blockages occur, the pump has to increase pressure. In the case of our circulatory system, when damage to the arteries occurs, a plaque (atherosclerosis) forms as a nice soft flexible band-aid, along with the cholesterol and other ingredients, but it is the calcium that moves out of the blood to form a hardened plaque. Unless the damage is halted and reversed, damaged areas begin to thicken and harden (from the calcium), forming an atherosclerotic plaque and building up pressure.

Unlike the pipes in the garden, our arteries are flexible tubes surrounded by a layer of muscle. When the heart pumps the blood, the arteries expand to take the extra liquid and contract to help push the liquid along the arteries. If the muscles surrounding the arteries are rigid and cannot relax and function properly the arteries can’t expand and push the blood away from the heart, so the heart again has to pump harder and pressure builds.

The major reason for the arteries not relaxing is the damage done to a thin layer on the inside of your blood vessels called the endothelium. This single, very fragile one-cell layer sends messages by a chemical called nitric oxide (NO) to relax the arteries. If this layer, the endothelium, is damaged or doesn’t have the ingredients to produce NO, the arteries cannot relax. In healthy people the cells of blood vessels release NO, which instructs smooth muscles surrounding arteries to relax. In this manner blood vessels can release their constriction by themselves and lower blood pressure. With increasing arterial damage from plaque, high blood pressure, acidosis,oxidation and inflammation, the ability to produce NO declines. Simple. Many of the blood pressure drugs on the market, including Viagra, work on the same NO principle but nutrition does it better and much, much more safely.

More than 97% of high blood pressure is therefore caused by (1) not enough water in the pipes so the blood becomes too viscous, (2) damage to the arteries caused by poor nutrition and lifestyle and (3) the muscles around the arteries and arteries not being able to relax because of poor nutrition and lifestyle. To reverse high blood pressure all it takes is the nutrients required to repair and maintain healthy, flexible arteries and enough liquid by drinking adequate quantities of good clean water. At least this is what the research shows.

Studies have shown blood pressure lowered by 10 or 20 points in a few weeks or less of supplementing with just one nutritional ingredient or dietary and lifestyle changes without any medication. In support of this I have met hundreds of people who have lowered their blood pressure within a few days to weeks by changes in nutrition and lifestyle including drinking more water. Most telling though, I recently met a nutritional doctor friend of mine who had a patient come to her on five different drugs to lower blood pressure. Not only were the drugs not working but also the patient was having serious side effects common to these drugs. My friend put her on a very simple nutritional regime and was able to get her off all the drugs and lower her blood pressure within two weeks. Nutrition and lifestyle factors are the main cause of hypertension and atherosclerosis; it makes sense, therefore, that changes in these must surely reverse the condition. Another person, “EM,” had a blood pressure reading of 153 and was on two different medications but was having side effects. She adopted my blood pressure smoothie (see later) and over three weeks dropped to 123 mm Hg. Her energy levels were up and she felt much better than she had in years.

Unfortunately despite the effectiveness of diet and lifestyle changes the health system most often resorts to medication and puts the fear of god into you if you don’t take the drugs. While many antihypertensive drugs have proven results in decreasing blood pressure, they are not addressing the problem and that they have serious, even deadly, side effects including heart attack, Alzheimer’s and weight gain which then lead to many other complications. Furthermore, patients treated for high blood pressure with drugs still have a higher risk of heart attack and stroke compared to the average population unless these patients change their diet and lifestyle. Just one example, and I have book full of them, shows that beta blockers, which are one of the first choice medicines for hypertension and while undoubtedly effective at lowering blood pressure, actually increase cardiovascular mortality in doing so. So they stop one problem to create another. A meta analysis of 22 randomized controlled trials evaluating 34,096 patients taking beta blockers against 30,139 patients taking other antihypertensive agents and 3,987 patients receiving placebos found that the use of beta blockers to lower heart rate in hypertensive individuals increased the risk of cardiovascular events and death for patients (Bangalore et al. 2008, J Am Coll Cardiol. 2008; 52(18):1482-1489). The latest research on aspirin also shows the benefits have been exaggerated and the side effects kept quiet to the point where many researchers are now saying there is no benefit of taking aspirin and in fact there may be harm. By contrast, Pycnogenol, an extract from grapes, have shown it inhibits platelet aggregation as easily and effectively as would a five-times-larger dose of aspirin (Colman et al. 1999) as have many other nutrients.

Put simply what does work is increased levels of fruit, nuts, vegetables, beans, supplementation, sunlight and physical activity and stress less and avoiding toxins. Apart from these the best approach for those seriously wanting to reduce their blood pressure is Dr Dingle’s Blood Pressure Smoothie. The reason I call it the blood pressure smoothie is all of the ingredients have been multiple shown in scientific studies to reduce blood pressure. By no way is this meant to replace advice from you GP but you can share it with them and see if they are interested in preventing the problem rather than just treating it with pharmaceuticals. Remember also that I am not a GP I am just the guy who does all the research which is why I have a PhD.

4 ingredients in order of importance
Almonds (soaked for at least 8 hours)
Linseed (flaxseed)
Filtered re-mineralised ionized water. 

Extras for taste and minerals

You will remember earlier how NO relaxes the muscles surrounding the arteries and many of the beneficial actions of nutrition on lowering blood pressure results both directly and indirectly through improving endothelial tissue and NO production and release from this tissue. Two major pathways to increase NO are increase the rates of nitrates in the diet, the building block for NO, and L-Arginine which stimulate the enzyme to manufacture NO. A third mechanism that is absolutely critical is to protect and repair the endothelium, remember it is only one cell thick and very susceptible to damage. Vitamin C and antioxidants are essential for this part.

Diets high in dietary nitrate such as beetroot are associated with reduced blood pressure increased exercise performance as a result of vasodilation (expansion) of the blood vessels and a decreased incidence in cardiovascular disease. 100-200mg of beetroot per day has been shown to produce immediate effects of lowering blood pressure by around 15 mm of Hg. High levels of nitrate can be found in spinach, fennel, radishes, parsley, aubergine (eggplant), squash, broccoli, cabbage and kale, chard, cucumber, fennel, garlic and onions, kohlrabi, pumpkin, radishes (especially black radish), spinach, beans, celery, rhubarb, with the highest level, over 3,500 mg/kg found in lettuce, especially iceberg, cos, arugula (rocket).

Almonds have one of the highest sources of L-Arginine (most nuts have lots of L-Arginine so you can substitute the almonds if you want) which stimulates NO synthesis. Studies of almonds have shown reductions of 5-6 mm of blood pressure. It is important to soak the almonds as they (all nuts and seeds) have enzyme-inhibiting factors in them which stop them from germinating until they have enough water. Flaxseed is rich in Omega 3 fatty acids, L Arginine (about 20% less than almonds), lignans, antioxidants and fiber that together probably provide benefits to patients with cardiovascular disease. Studies on consuming 30g of flaxseed have been shown to reduce blood pressure by up to 15 mm Hg.

The great thing about this smoothie is that you can add just about anything else you want to it and it will make it even tastier and better for you. If you want to make up your own to add just a bit more “ump” or new taste sensation try these below.

Hundreds of studies have shown many other food ingredients to lower blood pressure including green tea which has been shown to reduce blood pressure by 4-5 mm. Flavanols found in cocoa have been shown to increase the formation of endothelial nitric oxide. The Greeks, Egyptians and Romans effectively used garlic to treat a host of ailments including infections, digestive problems, and high blood pressure. In a study of 210 Patients with hypertension supplementing with garlic showed significant decrease in blood pressure in both dose and duration dependent manner. In fact the garlic treated group outperformed the drug Atenolol (a selective β1 receptor antagonist and one of the most widely used beta blockers to lower blood pressure) and the placebo. But don’t tell your GP this they wont believe it.

Without any doubt supplementing with L Arginine, an amino acid, can have dramatic and rapid results in lowering blood pressure. Often many times better than any combination of drugs and it is available in many health food stores. Although you can get L Arginine in Almonds and other nuts you get a lot more and faster benefits by supplementing. One person I know had a drop of more than 25 mmHg in a few days from just using L Arginine. Then when they added the smoothie their doctor took them off their blood pressure medication. In a meta analysis of 29 randomized, controlled, clinical trials investigating vitamin C intake they found that taking an average of 500 milligrams of vitamin C daily reduced blood pressure by around 4 mmHg. Among those diagnosed with hypertension, the drop was nearly 5 mm and more vitamin C led to even lower levels of blood pressure. I have more than 5g of vitamin C each day. Quercetin supplementation also reduces blood pressure by around 7 mmHg. Lycopene, which the red you get in tomatoes reduces blood pressure by around 5 mm. Further analysis showed that supplementing with higher dosage of lycopene supplement (>12 mg/day) could lower blood pressure more significantly, especially for participants with higher blood pressure. Coenzyme Q10 lowers blood pressure and is particularly effective in reducing hypertension in diabetics and that it not only lowers blood pressure but also improves diabetic control. Supplementation with a marine pine bark extract for 8 weeks statistical significantly lowered systolic blood pressure. Almost 60% of the patients who supplemented with a marine pine bark extract were able to cut their prescribed medication dosage by half to keep their blood pressure in a healthy range. Amongst the minerals implicated in heart health via blood pressure lowering or improvements in vascular health are magnesium, potassium and selenium. A number of studies have also shown that probiotics also contribute to lower blood pressure.

It is very clear that by adopting my blood pressure smoothie and having lots of the nutrients I have mentioned throughout the day you can have a real impact on lowering blood pressure without drugs. Many of the studies on foods have shown that the foods are able to out perform the drugs and have no negative side effects, but are so good for you they help in many areas of health including lowering your risk of some cancers and other forms of disease.

In the words of Hippocrates the father of medicine some 2000 years ago.

“Let food be thy medicine”

and in my words “you can also supplement too to get an even better result”



Dental Fluorosis

Dental fluorosis is a serious condition that affects the growth and development of tooth enamel, particularly in younger children. It is characterised by an increased porosity of the tooth enamel, coupled with visible discolouration (colouration can vary from small white spots to large brown and black stains) (Fomon. 2000). In severe cases fluorosis can lead to an extensive increase in the fragility of the teeth (leading to chipping, fracturing and pitting) and decay. In 2005 32% of American children (Australian data was unavailable) were diagnosed with mild cases of fluorosis (CDC. 2005). A study by the Ontario Ministry of Health and Long Term Care found that the rates of fluorosis in fluoridated communities were significantly higher than the rates from non-fluoridated communities, indicating that excess consumption of fluoride via water fluoridation was having a direct effect on dental health (Locker. 2005). 


The biology of dental fluorosis suggests that fluoride hinders the healthy development of tooth enamel by interfering with the mineralization (enamel ‘building’) process of growing teeth (Fejerskov et al. 1996). When a tooth is developing in a child’s gum a complex matrix of enamel rods (which will eventually become the outer layer of the tooth) is created (DenBesten. 2002). The building of these matrixes is organized by the protein known as amelogenin (Fejerskov et al. 1996). Typically, once the enamel matrixes have been formed, the amelogenin is broken down by a protease (enzyme that breaks down proteins), leaving room from the full mineralization of the tooth enamel (Aoba & Fejerskov. 2002). However, studies have demonstrated that fluoride interferes with the protease activity and inhibits the enzyme from breaking down all of the amelogenin (ATSDR. 2003). Therefore, following mineralization where the enamel matrixes are mineralized by calcium crystals to produce completely formed enamel, a tooth which has been exposed to fluoride will appear porous, due to the retention of amelogenin and the incomplete mineralization of the enamel (DenBesten. 2002). However, teeth are not the only body part susceptible to the toxic effect of fluoride, skeletal fluorosis is another emerging health condition related to excess consumption of fluoride. 




Antidepressants Don’t Work

Depression is a debilitating condition and a major public health problem. It is the top-ranking cause of non-fatal disease burden in Australia, accounting for eight percent of the total years lost due to disability in 1996 [1]. It is predicted to be the second largest cause of disability in Australia by the year 2020 [2]. Depression is a mental disorder that has the potential to greatly impact one’s everyday activities. The experience of depressed mood, insomnia, loss of energy, irritability and other symptoms are commonly linked with depression. Further, recent research demonstrates its association with inflammation.

Unfortunately, although we continue to diagnose and medicate people for depression, there is little science and certainly no evidence to continue to prescribe antidepressants to most individuals. There are more myths in this area than there are facts and, as a result, many people are led astray by an industry that makes huge amounts of money from people’s suffering.

Depression theory

It is important to understand that most of what we know about the biochemistry and physiology of depression is theory and not fact. It is a hypothesis but is often presented by professionals as truth, with the connotation that these professionals know the full truth about depression. No, in fact, they do not. What we do know is that serotonin is located in the pineal gland, blood platelets, the digestive tract and the brain. Serotonin acts as a chemical messenger that transmits nerve signals between nerve cells and also causes blood vessels to narrow [3]. We know that there are many other chemical messengers in the body that can have an impact on our mood and state of wellbeing.

Traditionally it has been thought that drugs most commonly used to treat depression—the selective serotonin reuptake inhibitors (SSRIs) such as Prozac® and Zoloft®—act according to the serotonin hypothesis. This hypothesis purports that levels of serotonin in the brain determine how we feel: high levels of serotonin cause heightened happiness, while decreased levels lead to sadness. Clinical depression has been attributed to low levels of serotonin transmission in the brain [4]. The serotonin transporter 5-HT is a reuptake molecule that removes serotonin, so it is thought that the SSRIs act to interfere with the action of 5-HT and therefore allow serotonin to accumulate and levels to increase [4]. This theory is still strongly supported by the pharmaceutical industry [5], which even uses it to encourage people to “correct” their serotonin levels in advertising for the drugs [6].

More recently, this theory has received much criticism as neuroscience research has failed to confirm “any serotonergic lesion in any mental disorder” 6. That is, the theory is just not supported by evidence. A growing body of research disagrees with the serotonin hypothesis [6][7][8]. In support of this, a Cochrane review found that tricyclic antidepressants are of the same efficacy as SSRIs [8]. Since tricyclics do not impact serotonin levels, this would suggest that the serotonin hypothesis has been disproved. But someone forgot to tell the drug companies and professionals who continue to aggressively dish out these drugs.

Despite the blind acceptance of the serotonin theory, the GlaxoSmithKline website has posted: “There is no clear cut reason for depression, and a number of factors may be at play, including altered levels of chemical messengers (neurotransmitters) in the brain, such as serotonin and noradrenaline” [9]. If antidepressants were a cure for depression, there would be a definite illness, with definitive symptoms and causes that the drugs are targeting. GlaxoSmithKline’s statement does not support this case.

Antidepressants describe the broad range of medications prescribed to alleviate the symptoms of certain depression- and anxiety-related mood disorders and include a number of different groups of medications. These include monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), tetracyclic antidepressants (TeCAs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and the current standard treatment group: selective serotonin reuptake inhibitors (SSRIs), which became immensely popular in the 1990s [10].

The first antidepressant that came along with a huge fanfare was Prozac®. Prozac® appeared on the market in 1988 and is still being prescribed today. It has become one of the most prescribed drugs to date [11]. Prozac® is part of a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs).

The prescription of antidepressants has skyrocketed over recent decades 10. From 1996 to 2005, individuals treated with antidepressants became more likely to also receive treatment with antipsychotic medications and less likely to undergo psychotherapy—the net result is more drugs and less treatment. The percentage of the U.S. population using at least one psychotropic medication increased from 5.9% in 1996 to 8.1% in 2001 [12]. Among the psychotropic drugs, antidepressants are the most frequently prescribed medications. The U.S. CDC found that antidepressant use in the United States jumped nearly 400% by the 2005-2008 survey period, compared with the 1988-1994 period, with 11% of those over age 12 taking the drugs (U.S. CDC and Prevention’s National Center for Health Statistics) up from six percent in 1996 [13].

Antidepressants are now used by more than 27 million Americans, most of whom are women [14]. Women are twice as likely as men to be diagnosed with major depressive disorder and up to three times more likely to be diagnosed with dysthymic disorder [15]. However, despite the absence of any scientific evidence, antidepressants are increasingly being prescribed for other conditions such as hot flashes, headache, back pain, neuropathy, sleep-related conditions, anxiety spectrum disorders, eating disorders and fibromyalgia [16]. Once prescribed, many people continue taking antidepressants, with more than 60% of Americans who use the drugs reporting being on them for two years or more. And about 14% of Americans taking antidepressant medication have done so for 10 years or longer. Patients who take the drugs often get them from their regular doctor rather than a so-called mental health professional.

Last year in Australia, there were 29 million prescriptions written for medications related to mental health issues. Antidepressant medications accounted for nearly 60% of these scripts, followed by anti-anxiety and anti-psychotic drugs [17]. This suggests that around 2.4 million Australians are using medication to deal with mental health issues.

In the United States, “The number of visits by patients for depression was 24.5 million in 2001, a 70% increase since 1987” [18]. The ambiguous nature of depression has provided leeway for significant misdiagnosis. The difficulty in identifying valid cases of depressive disorder lies within its tendency to share unclear boundaries with other mental disorders and normality [19]. The distinction between major depression and sadness, for instance, has become completely obscure. Previously, depression was classed as either endogenous or reactive [19]. Endogenous depression was regarded as a rare biological condition, whereas reactive depression was exogenous and triggered by stressful events outside our control, such as the loss of a loved one [19].

Under the Diagnostic and Statistical Manual (DSM-III), the diagnosis of clinical depression requires the presence of at least five of the possible nine symptoms for at least two weeks. Some of these symptoms include loss of interest in usual activities, depressed mood, fatigue, insomnia and lowered appetite. Yet many of these symptoms can be seen in natural responses to stress, loss [19], illness, fatigue and poor sleep. Unfortunately this weak criterion translates into a “low threshold for diagnosing clinical depression” [20]. This suggests that there are huge risks in misdiagnosing normal emotional states as clinical illnesses. As an example, chronic fatigue is also commonly mistaken for depression due to the large overlap in symptoms. In one study involving 3,200 individuals, patients who were depressed in the beginning of the study were found to be four times more likely to be fatigued, rather than “depressed” [21]. Alas, due to the reinforcing nature of depression and fatigue, diagnosis becomes difficult.

Considering the major ambiguities surrounding the concept of depression, it is not surprising that the quantity of prescriptions for antidepressant medication is so high. What is of most concern is the number of people who are taking antidepressants and exposing themselves to unnecessary risk and, in too many cases, are not taking action to resolve underlying issues.

In 2002, a group of researchers studying the “placebo effect” compared studies on those taking sugar pills (placebo) and those taking antidepressants—a group of drugs the researchers expected to be effective—and found the opposite of what they expected. The meta analysis, written by Professor Irving Kirsch, was titled “The Emperor’s New Drugs: An Analysis of Antidepressant Medication Data Submitted to the U.S. Food and Drug Administration.” Kirsch obtained data from the FDA and reported that antidepressants were no more effective than a placebo. However, he did state that antidepressants might have a small effect and that in severe depression the placebo did not function as well as normal while the drug did show some efficacy [22]. Professor Kirsch has also published a book of the same title (The Emperor’s New Drugs) that is well worth reading.

In a later analysis of additional data, Kirsch supported his earlier findings and reported antidepressants may be more effective than a placebo only in severe depression [23]. Now with more than a dozen major meta analyses, the research continues to show there is little supporting evidence that antidepressants work when placebos appear to be just as—and in some case more—effective. The research also shows the long-term effects tend to be severe [22][23][24][25][26][27]. In the majority of studies, antidepressants performed the same as inactive placebo pills.

A recent study found that a minority of antidepressant users actually fared worse than placebo users. In this study, researchers randomly assigned 156 depression patients to either take the antidepressant sertraline (Zoloft® and other brands) daily for 16 weeks or be in a placebo group given inactive pills. After 16 weeks, there were no overall differences in how the groups fared 28. Of the antidepressant patients, 31% were treatment “responders,” meaning they had fallen below a certain score on a standard measure of depression symptoms, or had seen their score drop at least 50%. The same was true of about 28% of patients in the talk-therapy group, and 24% in the placebo group. The differences among the three groups were so small as to likely be due to chance [28].

Two even bigger reviews in 2010 came to the same conclusions. A review of four meta analyses of efficacy trials submitted to the U.S. Food and Drug Administration (FDA) suggests that antidepressants are only “marginally efficacious” compared with placebo and “document profound publication bias that inflates their apparent efficacy.” In addition, when the researchers analysed the largest antidepressant effectiveness trial ever conducted, they found that “the effectiveness of antidepressant therapies was probably even lower than the modest one reported... with an apparent progressively increasing dropout rate across each study phase” due to side effects [29]. A review of nine studies involving 751 participants found that, from the results presented, antidepressants had only a small positive effect when compared to an active placebo [30]. Other studies have also shown St John’s Wort to be more effective than an SSRI [31] and exercise to be at least as effective in older patients [32].

Other irregularities were seen in the data. It was noted that published data consisted entirely of positive outcomes and that many of the negative trials’ reports were not published or that negative data were displayed in a positive manner [25][26].  Publication bias, where only the positive results are reported and published, is well known in the drug industry and just a part of the drug companies’ everyday lies and deception.

Despite the findings of researchers, the FDA in the U.S. reports that 94% of its studies have shown positive results, with antidepressants found to be effective in treating depression [33]. However, publication of antidepressant studies by the FDA is highly selective: “The studies that the FDA judged as positive were approximately 12 times as likely to be published in a way that agreed with the FDA analysis as were studies with non-positive results according to the FDA” (Turner et al. 2008). Why have the FDA in the U.S. and Australian regulatory authorities continued to go against the scientific evidence?

The likely benefit of antidepressants is the placebo effect [23][25]. In trials, the patients on placebos would see the doctor on a weekly basis for check-ups and to update the analysts for the report. In addition, the patients were within easy access to help 24 hours a day [26][34]. Thus, the amount of human contact, attention and care skews the results [26]. This could possibly reveal the reason the placebo had such a strong effect. Imagine the positive feeling from being closely cared for by your medical practitioner, including having his or her phone number, rather than just in and out of the office in 12 minutes. The amount of attention and care influenced the strength of the placebo. Under real-world conditions, the patient sees the doctor less frequently and is less likely to seek help [26][34].

The actual efficacy of SSRIs, therefore, remains in question and often subject to the merits and interests of those conducting a particular study. Many people drop out of drug trials because of the seriousness of side effects. The serotonin receptors are responsible for a variety of functions unrelated to mood, such as sleep, appetite and sexual function, as well as symptoms such as pain, nausea, depression, and anxiety [35]. Common side effects of taking an SSRI include nausea, dizziness, gastrointestinal disturbances, anxiety, agitation, insomnia, sexual dysfunction and weight gain 35. Significant literature exists documenting the symptoms of SSRI discontinuation syndrome, which range from moderate to severe [36]. There can also be more serious consequences: SSRI use has been linked to serotonin syndrome, birth defects and high risk of suicide. The link between antidepressants and suicide has been recognised for at least 20 years and the United States FDA requires that antidepressants carry a label warning of this increased risk on each box [37]. In such cases it would seem antidepressants are not effective at all and, in fact, can have serious and even deadly side effects.

Despite these findings that have now been repeated many times, “professionals” working in the field still state that antidepressants work and continue to prescribe them to more and more people.

It is also worth pointing out that in the United States, until 1990 tryptophan dietary supplements were being taken by approximately 15 million Americans. On March 22, 1990, the Food and Drug Administration (FDA) banned the sale of L‑tryptophan in response to several deaths during the previous year from a deadly flu‑like condition called EMS [38]. This is despite L-tryptophan having been used as a supplement for decades prior to this, by a large number of people, without any adverse side effects. The problem was caused by a contaminated batch of tryptophan, not the tryptophan itself. One wonders why it was banned, as most drugs including antidepressants would be removed from the marketplace if this principle were applied across the board, including drugs that have been linked with hundreds of thousands of deaths.

However, on March 26, 1990, only four days after the banning of L-tryptophan, Prozac®, the wonder drug in the treatment of depression, was introduced with great fanfare after more than 10 years of development. What a coincidence. As mentioned earlier, Prozac® is an SSRI, whilst tryptophan actually increases the serotonin levels in the body.

Other interesting facts about this controversy:

L‑tryptophan was banned as a dietary supplement in the United States and Australia until 2005. It could, however, be imported from Japan and became available as a prescription-only drug. One hundred 500 mg capsules cost approximately $75.00. This is about five times more expensive than its previous cost as a dietary supplement.

L‑tryptophan is still used in baby food produced and sold in the United States.

Farmers are still allowed to use it in stock feed for animals. I wonder if this is because happy animals are more likely to gain weight?

  1. [1]Mathers et al. 2000
  2. [2]Minas et al. 2007
  3. [3]MedicineNet 2003
  4. [4]Schafer 1999
  5. [5]Cowen 2008
  6. [6]Lacasse and Leo 2005
  7. [7]Murphy 1998
  8. [8]Geddes et al. 2005
  9. [9]GlaxoSmithKline 2008
  10. [10]Olfsen et al. 1998
  11. [11]Wrobel 2007
  12. [12]Zuvekas 2005  
  13. [13]Olfson et al. 2009
  14. [14]Cosgrove et al.
  15. [15]American Psychiatric Association 2000
  16. [16]Roberts 2007
  17. [17]Australian Institute of Health and Welfare
  18. [18]Fergusson et al. 2006
  19. [19]Parker 2007
  20. [20]Lucassen et al. 2007
  21. [21]Skapinakis 2004
  22. [22]Kirsch 2002
  23. [23]Johnson and Kirsch 2008
  24. [24]Kirsch and Moncrieff 2005
  25. [25]Ioannidis et al 2008
  26. [26]Posternak and Zimmerman 2007
  27. [27]Crawford and Parker 2007
  28. [28]Barber 2011
  29. [29]Pigott et al. 2010
  30. [30]Moncrieff et al. 2010
  31. [31]Szegedi et al. 2005
  32. [32]Blumenthal et al. 1999
  33. [33]Turner et al. 2008
  34. [34]Blier 2008;
  35. [35]Ferguson 2001
  36. [36]Haddad 1998
  37. [37]Reeves and Ladner 2010
  38. [38]Manders 1995



Shannon Fitzgerald , Ben Gundry, Kahlia Belli, Noratiah Larry, Grant Swan and Jan van der Walt, Geraldine Treloar



Sitting disease

Sitting for any length of time may not be good for us, as more and more evidence shows that sedentary behaviours including sitting, watching television, using a computer, and driving a car are risk factors, independent of physical activity, for adverse chronic disease in adults such as obesity, cancer, heart and kidney disease, chronic neck and back pain, as well as premature death. The act of sitting increase your chances of developing all this conditions independent of how much exercise and active you are outside of sitting. You can do a long run every night, but if you sit too long during the day you still increase your risk of these chronic conditions. Unfortunately people have grown more sedentary during the twentieth and twenty-first centuries. On average adults spend an average of 8 hours per day sitting, increasing to 10 or more hours a day in older age and young people between the age of 6 and 20 spend on average 40 to 60% of the day sitting, often in prolonged and uninterrupted bouts [1]. In Australia, at least according to the ABS we sit (sedentary) for around 39 hours a week and on average 10 hours at work. But these are average and clerical and administration workers have an average of 22 hours sitting at work. Apparently we sit for 13 hours a week in front of television and sitting in front of a computer for non-work related activities 8 to 24 year old sit for 9 hours a week. Remember these are just averages and as I don’t sit down much (standing desk) someone is sitting a lot more than average. Also however, people who tend to sit at work also tend to sit more in other locations adding to the increased burden of sitting.



Studies have linked sitting to a greater risk for colon, prostate, breast and endometrial cancers. In a review of 18 studies ten found statistically significant, positive associations between sedentary behavior and cancer outcomes. Sedentary behaviour was associated with increased colorectal, endometrial, ovarian, and prostate cancer risk; cancer mortality in women; and weight gain in colorectal cancer survivors [2]. In a study of 5380 women and 5788 men a standing/walking occupation was associated with a 32% lower risk of all-cause mortality and a 40% risk reduction in cancer mortality, compared to sitting occupations. Too much sitting is also associated with cancer survival. Sitting is associated with weight gain around the waist, insulin resistance, and markers of inflammation which may contribute to adverse cancer outcomes (disease progression, recurrence, or death) and to the development of other chronic disease. The daily sedentary time was correlated with the protein levels of inflammatory biomarkers [3] [4] [5] which is associated with cancer incidence and survival. Initial studies indicate that cancer survivors spend two-thirds of their waking hours sitting [6].


A number of studies have now found that ownership of a car and a TV was associated with an increased risk of heart attack [7] [8]. Several in-depth studies have reported television-viewing time to be detrimentally associated with weight gain, type 2 diabetes mellitus, some cancers, abnormal glucose metabolism, metabolic syndrome, and other cardiovascular risk factors. According to American Council on Exercise, every hour you sit in front of the television, your life expectancy is slashed by 22 minutes. Watching television for six hours a day takes five years off your life. People who watched the most TV in an 8.5-year study had a 61% greater risk of dying than those who watched less than one hour per day. In a study of 8,800 adults 25 years of age or older, each extra hour of television watching per day was associated with an 18% increase in deaths from heart disease and an 11% increase in overall mortality. People who watched TV for at least four hours a day were 80% more likely to die of cardiovascular disease than those who watched two hours or less, and 46% more likely to die of any cause [9]. In a study that included 61,395 men and 73,201 women aged 45 to 75 years, the longest sitting duration, 10 or more hours each day compared to five or less hours a day, was associated with increased all-cause  (dying of anything)(11%) and cardiovascular (19%) mortality. The risk of five hours each day compared to one hour each day of sitting and watching TV were 19% in men and 32% for all-cause mortality [10]. A review of prospective studies of screen time (TV and computer) and sitting time has shown that greater sedentary time is associated with an increased risk of fatal and non-fatal cardio vascular disease (CVD). Compared with the lowest levels of sedentary time, risk estimates ranged up to a 68% increase for the highest level of sitting time and 125% increase for the highest level of screen time. In six studies of screen time, for each two hours of sitting there was a 17% increase risk of CVD. However in two studies, the increased risk of CVD was 5% for each extra two hours of sitting in front of a screen [11].

In a study of 2,761 women and 2,103 men without clinically diagnosed diabetes, sitting time was detrimentally associated with waist circumference, BMI (body mass index), weight gain, blood pressure, fasting blood fats, HDL cholesterol, two-hour postload plasma glucose, and fasting insulin in both men and women. TV viewing time was detrimentally associated with all metabolic measures in women and all except HDL cholesterol and blood pressure in men [12]. An analysis of 18 studies including a total of 794,577 participants found that those who sat for long periods of time compared with the lowest sitting time was associated with a 112% increase in the risk of diabetes, a 147% increase in the risk of cardiovascular events, a 90% increase in the risk of cardiovascular mortality and a 49% increase in the risk of all-cause mortality [13]. In a study of 222,497 individuals 45 years or older the risk of all-cause mortality (any type of death) increased by two percent for those sitting for four to eight hours, 15% for eight to 11 hours and 40% for those sitting more than 11 hours a day compared to less than four hours each day and was independent of physical activity levels [14] [15] [16].


Sitting is also a risk factor for weight gain and diabetes. That is, the more you sit the greater the risk of developing theses conditions independent of other activities. In a meta-analysis using 48 studies, a consistent relationship of self-reported sedentary behaviour with mortality was found with weight gain from childhood to the adult years [17]. That is, the greater the sedentary time in childhood, the greater the weight gain. In a cross-sectional study of 8,357 adults aged 35 years or more and free from diabetes, time spent watching television for women was positively associated with increased 2 hour plasma glucose, fasting insulin, and insulin resistance and pancreas Beta cell function. These findings highlight the unique negative relationship of sedentary behaviour of television viewing time and glycaemic measures independent of physical activity time and weight and suggest an important role for reducing sedentary behaviour in the prevention of type 2 diabetes and cardiovascular disease, especially in women [18].

In theory, this may be in part because non-exercise activity is a much greater component of total daily body energy expenditure than exercise or because any type of brief, yet frequent, muscular contraction throughout the day—such as standing or moving—may create healthy molecular signals which positively alter the body’s biochemistry and metabolism. One of these is a particular muscle chemicals, lipoprotein lipase (LPL), a protein enzyme has been studied in depth because this enzyme has a central role in several aspects of lipid (fat) metabolism [19] [20]. LPL controls plasma triglyceride (fat) breakdown (burning the fat into energy), shifting the cholesterol from LDL to HDL and other metabolic risk factors decrease when we stand or are involved in physical activity. Experimentally reducing movement by sitting had a much greater negative effect on LPL regulation than a positive effect of adding vigorous exercise training on top of the normal level of nonexercise activity [21]. Within a couple hours of sitting, HDL cholesterol drops by 20% [22]. This suggests that, at a minimum, we don’t need to exercise regularly but we do need to be breaking up our sitting time, probably every 20 or 30 minutes. In support of this, rat studies also show that the amount of time we are sedentary influences how our bodies process fats given that leg muscles only produce the lipase lipoprotein (LPL) fat-processing molecule when they are being actively flexed, either standing or moving. The importance of producing enough LPL cannot be underestimated as a meta-analysis of 29 separate studies with 20,903 participants who have a specific genetic type (polymorphism) that creates less LPL was associated with a five-fold increase in the risk for death and greater chronic heart disease [23]. The production of LPL is therefore extremely beneficial to us.


Standing up

A growing body of evidence suggests that simply standing up (independent of total sedentary time and moderate-to-vigorous intensity activity) reduces the risk of coronary heart disease [24]. By limiting the time spent sitting, the risk of diabetes, heart disease and death can be reduced dramatically. It is important to take breaks from long periods of sitting down, such as taking a walk during your lunch break and taking a break from work at the computer or having a standing desk [25]. Just taking breaks or increasing standing time has a significant benefit on blood biochemistry. Researchers found levels of C-peptide, which is involved in the synthesis of insulin, were significantly lower during interrupted sitting compared with prolonged sitting. In another study independent of total sedentary time and moderate-to-vigorous intensity activity time, increased breaks in sedentary time were beneficially associated with waist circumference, body mass index, triglycerides, and 2-hour plasma glucose [26]. While in a study of 70 adults involving sitting for nine hours, regular activity breaks lowered plasma insulin levels and lowered plasma glucose when compared with prolonged sitting, even when compared with physical activity. While physical activity lowered plasma triglyceride more with regular activity breaks, activity breaks were more effective than continuous physical activity at decreasing negative blood sugar and insulin levels in healthy, normal-weight adults [27].

Overall, there is a compelling case for sitting reduction to be included in clinical preventive advice as a key component of “active living,” where adults and children are encouraged to “stand up, move more and sit less” across different settings and locations throughout the day. Just standing up every 20 or 30 minutes can have a remarkable health benefit reducing your risk of many chronic illnesses. How simple is that.


  1. [1] Matthews et al 2008.
  2. [2] Lynch et al 2010
  3. [3] Tohoku et al 2014
  4. [4] Yu et al 2011
  5. [5] Lynch BM et al 2011
  6. [6] Lynch et al 2013
  7. [7] Owen et al. 2010
  8. [8] Held et al 2012
  9. [9] Dunstan, et al. 2010
  10. [10] Kim et al. 2013,
  11. [11] Ford and Caspersen 2012
  12. [12] Thorp et al. 2010
  13. [13] Wilmot, et al. 2012
  14. [14] van der Ploeg et al. 2012
  15. [15] Katzmarzyk et al. 2009
  16. [16] Dunstan et al. 2011
  17. [17] Thorp et al. 2011
  18. [18] Dunstan et al. et al. 2007
  19. [19] Olivecrona et al. 1997
  20. [20] Goldberg and Merkel 2001
  21. [21] Hamilton et al. 2007
  22. [22] Bey and Hamilton 2003
  23. [23] Wittup et al. 1999
  24. [24] Dunstan et al. 2011
  25. [25] Helajärvi et al. 2013
  26. [26] Healy et al. 2008
  27. [27] Peddie et al. 2013

Our environment CVD and weight gain

Our environment is where we live. In fact, the word “environment” has its roots in fourteenth-century Middle English and means, “that which surrounds us.” The biggest advances in our health and longevity are the result of improvements in our environment—not through medication, despite what we are often led to believe. There’s overwhelming scientific evidence (and it’s also common sense) that if you have a sick environment, you are also likely to be sick.

Environmental factors generally receive little attention concerning how they influence the development of cardiovascular disease yet they can play a major role. Large numbers of studies now implicate environmental toxins, particularly air pollution and persistent organic pollutants (POP’s), in many of the risk factors associated with CVD, including high blood pressure, heart attacks, strokes and even Alzheimer’s disease.


Considerable evidence exists to prove that air pollution contributes to inflammation and oxidation throughout the body and, in turn, leads to an increased risk of heart attack, stroke, heart failure and a number of chronic diseases including diabetes and asthma. Put simply, air pollution has a similar effect on blood vessels as smoking cigarettes. Air pollution from traffic and other sources is an established cause of premature mortality.[1] Acute events such as heart attack or stroke can be triggered by short-term exposure to air pollution.[2]

Exposure to air pollutants, particularly pollutants caused by motor traffic, increases the risk of a fatal heart attacks.[3] These environmental agents can influence the heart, as they can change a person’s heart rate and rhythm, alter the heart’s excitability and the contractibility of heart muscle, and cause atherosclerosis.[4] The association between air pollution and intima media thickness (IMT), an established marker of subclinical atherosclerosis, was reported for the first time in volunteers participating in two clinical trials in California.[5] Two population-based cross-sectional analyses[6] also reported associations between air pollution and IMT.

A study of 2,780 participants found indicators of air pollution nitrogen dioxide (25 µg/m3), traffic intensity on the nearest street (15,000 vehicles/day), and traffic load within 100 meters were associated with increased intima media thickness (IMT).[7]

Many observational studies in humans have found that within hours to days following exposure to air pollution, blood pressure increases. In animals, a 10-week study of hypertensive rats found that short-term exposure to air pollution elevates blood pressure in rats already predisposed to the condition.[8] Other studies have shown that diesel exhaust inhalation causes cardiovascular dysfunction including impaired vascular reactivity, increased blood pressure, and arterial stiffness. It is now well established that diesel exhaust inhalation disturbs normal vascular homeostasis and NO generation, which is involved in relaxing the artery wall muscles.[9]

Scientific studies have shown that air pollution is particularly hazardous to people with pre-existing cardiopulmonary diseases. Many studies already have linked fine particulate matter—which comes largely from vehicles and industries that burn fossil fuels—to heart risks and increased risk of premature death from cardiopulmonary disease,[10] including heart disease, insulin resistance (IR) and diabetes—all conditions that are characterized by inflammation. Particulate air pollution can exacerbate an individual’s risk of heart failure through a variety of mechanisms. Factors that enhance the clotting of blood are increased, as are fibrinogen levels and platelet aggregation. With particulate matter exposure, the viscosity of blood also increases. The variability of heart rate declines, which leads to arrhythmias. These factors may ultimately lead to an elevation in the incidence of heart disease.[11]

A number of studies have found a consistent and significant relationship between prevalence of type 2 diabetes and exposure to air pollution, especially ultrafine particulate matter.[12] Other studies have found that people who live in areas with high levels of traffic-related air pollution may face an increased risk of developing diabetes. After studying 52,000 residents of Denmark, researchers found that people living in urban areas with high levels of traffic pollution were four percent more likely to be diagnosed with diabetes than people living in neighbourhoods with cleaner air. The results suggest that air pollution may actually contribute to the development of diabetes. The link between long-term exposure to air pollution and diabetes also appeared to be greater in women. In an earlier study, the same researchers reported that people who live in areas with high levels of traffic-related pollution also might be at a slightly increased risk of dying from stroke.[13]

Those with enhanced susceptibility to the toxicity of air pollutants may include individuals with metabolic syndrome; the link between morbidity and mortality due to diabetes and exposure to ambient air pollution is well documented.[14] For example, exposure to PM2.5 (small particle matter less than 2.5 micron- 0.0025 mm) is associated with enhanced vascular reactivity[15] and cardiac function abnormalities[16] in diabetics. Acute cardiovascular responses to ozone (O3) exposure are also exaggerated, with increased heart rate (HR)[17] and decreased blood pressure (BP).[18] In addition, obesity and hypertension, common comorbidities of both metabolic syndrome and diabetes, are themselves susceptibility factors for adverse responses to PM2.5.[19] In epidemiological studies, elevated ambient concentrations of PM2.5 or carbon monoxide are linked to greater decreases in heart rate variability in metabolic syndrome subjects compared to healthy subjects.[20] In addition, small increases in urban ambient PM2.5 can decrease insulin sensitivity in healthy subjects,[21] suggesting that PM2.5 may contribute to the cause of metabolic syndrome or to the progression from metabolic syndrome to diabetes. Given the high prevalence of metabolic syndrome, the cardiovascular and metabolic health risk of exposure to ambient pollutants may be substantial.

Similar results have also been documented in animal studies. Rats that had induced metabolic syndrome (hypertensive and insulin resistant, and had elevated fasting levels of blood glucose and triglycerides) had more pronounced changes in heart rate and blood pressure compared to normal rats. The changes were also greater and more persistent, and lasted longer, in metabolic syndrome rats compared with those fed a normal diet.[22] These results in rodents suggest that people with metabolic syndrome may be prone to similar exaggerated blood pressure and heart rate responses to inhaled air pollutants. Animal studies have also found early exposure to ultrafine particulates led to the accumulation of abdominal fat, insulin resistance and increased inflammation in mice even if they ate a normal diet.[23] The study compared mice fed a high-fat diet with those fed a normal, healthy diet, and exposed some members of each group daily to ultrafine particulate matter. In the end, all of the mice exposed to air pollution, including those fed a normal diet, had increased abdominal and subcutaneous (under the skin) fat. These findings suggest that fine particulate pollution exposure alone, in the presence of a normal or high-fat diet, may lead to an increase in fat cell size and number, and also have a proinflammatory effect. The data also suggest a high-fat diet may exacerbate the health effects of inhaled PM2.5; therefore obese people also appear to be at increased risk.

Breathing large particles, not just small (PM2.5), also seems to affect the heart. People in a rural community experienced changes in their blood pressure and heart rates when they inhaled unfiltered local air that contained large particles, mostly from windblown dust and soil. In a controlled laboratory study of 32 adults in a chamber, volunteers inhaling unfiltered air had increased blood pressure (both systolic and diastolic). Blood pressure increased linearly every 10 minutes, and the subjects’ heart rates were elevated compared to the times they inhaled the filtered air.[24]

Animal studies link exposure to combustion hydrocarbon products from fossil fuels called PAHs (poly-aromatic hydrocarbons) to inflammation and subsequent development of diabetes mellitus. In addition, occupational studies suggest that exposure to PAHs may be associated with diabetes risk in humans. In a large US population-based study, researchers found a positive association between urinary biomarkers of PAH and diabetes mellitus. Compared to participants with the lowest PAH biomarkers, the risk of diabetes mellitus among those with the highest exposure was 3.1, or 310%, higher.[25] In another large observational study, researchers found exposure to PAHs was associated with increased heart rate variability.[26]


Persistent organic pollutants

In recent years, studies have increasingly associated exposure to environmental pollutants such as persistent organic pollutants (POPs) like PCBs, dioxin and pesticides to cardiovascular problems, including high blood pressure, heart attack and diabetes. In one study of 1,016 adults age 70 or older, seven of the POPs studied were significantly associated with the number of carotid arteries plaques, even after adjustment for multiple risk factors.[27] People with relatively high levels of certain pesticides in their blood have an increased risk of type 2 diabetes, particularly if they are overweight. In a study of approximately 2,000 older adults, the risk was higher among people with the highest levels of organochlorine pesticides in their blood. Those with levels in the top 10% were about twice as likely to have diabetes as their counterparts in the bottom 10%, but only in people who were overweight or obese. It seems that pollutants and body fat “may have a synergistic effect on the risk of type 2 diabetes.”[28]

There is emerging evidence that exposure to persistent organic pollutants (POPs) also plays an important role in weight gain. Blood serum levels of POPs, such as polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and organochlorine pesticides have been associated with increasing body mass index, elevated triglyceride levels, abdominal obesity, and cardiovascular diseases.[29] In animal studies, POPs have been associated with body weight gain, insulin resistance, abdominal obesity, hepatosteatosis (fatty liver) and atherosclerosis.[30] “Obesogens” (chemicals that increase the risk of obesity) are hypothesized to be environmental chemicals that promote obesity directly by increasing adipocyte size and/or number, or indirectly by altering metabolic homeostasis or interfering with regulation of appetite and satiety, suggesting that environmental chemicals can regulate lipid metabolism and adipogenesis, and thus promote obesity.[31] Hexabromocyclododecane (HBCD) is an additive flame retardant used in the textile industry and polystyrene foam manufacturing. Because of its lipophilicity (ability to dissolve in fats) and persistency, HBCD accumulates in adipose tissue and thus has the potential to cause metabolic disorders through disruption of lipid and glucose homeostasis. Mice fed a diet high in HBCD (700 μg/kg) and medium-dose of HBCD (35 μg/kg) had markedly increased body and liver weight. This effect was more prominent in the high-dose group. The findings suggest that HBCD may contribute to the enhancement of diet-induced body weight gain and metabolic dysfunction through disruption of lipid and glucose homeostasis, resulting in accelerated progression of obesity.[32]

Research also shows a link between prenatal exposure to persistent organic pollutants and weight gain in children.[33] Children exposed to certain persistent chemicals in the womb have a higher risk of being overweight. The results add to growing evidence that suggests POPs—by acting as endocrine disruptors—can influence weight gain. The developing foetus is exposed to POPs passed from the mother through the placenta. In a study of 344 children on Island of Menorca, researchers found that both PCB and DDE exposure led to an increased risk of weight gain in children as assessed by BMI scores. The link between being overweight and PCB and DDE levels in cord blood was stronger in girls than boys. DDT was associated only with weight gain in boys, especially in children with average or above-average fat intakes. In some cases, children with higher POPs exposures were almost twice as likely to be overweight compared to children with lower exposures, depending on the pollutant and the child’s gender.



Bisphenol A (BPA) is an industrial chemical that has become ubiquitous in its use in water bottles, food cans and even dental sealants. Higher levels of urinary Bisphenol A (BPA) are associated with cardiovascular disease, type 2 diabetes and liver-enzyme abnormalities. In a study, a very small increase in BPA concentration was associated with a 39% increased risk of cardiovascular disease (angina, coronary heart disease, or heart attack combined) and diabetes. Participants in the highest BPA concentration had nearly three times the risk of cardiovascular disease compared with those in the lowest concentration. Similarly, those in the highest BPA concentration had 2.4 times the risk of diabetes compared with those in the lowest. In addition, higher BPA concentrations were associated with clinically abnormal concentrations for three liver enzymes.[34]

Research has shown that BPA can interfere with cardiac rhythm. Parts-per-trillion concentrations of BPA triggered heart-muscle cells to begin beating to their own internal drummers. BPA mimics the hormone oestrogen in the body. The researchers linked this finding to oestrogen’s effect on calcium, which plays a pivotal role in heart-cell contractions. Both oestrogen and BPA—especially together—fostered a leakiness of calcium within female heart cells.[35] Researchers reported that delivering equal doses of oestrogen and BPA increased the cardiac effect more than would be the case from doubling the dose of either alone.

Since worldwide BPA production has now reached approximately seven billion pounds per year, eliminating direct exposures from its use in food and beverage containers will prove far easier than finding solutions for the massive worldwide contamination. Already many countries have taken steps to minimise BPA exposure.




[1] Brook et al. 2010.

[2] Ibid.

[3] Karolinska Institute 2005.

[4] Schwartz and Morris 1995.

[5] Künzli et al. 2005.

[6] Bauer et al. 2010; Diez Roux et al. 2008.

[7] Rivera et al.; Künzli et al. 2010.

[8] Sun et al. 2008.

[9] Langrish et al. 2013.

[10] Schwartz and Morris 1995.

[11] Ibid.

[12] Pearson 2010.

[13] Diabetes Care, online November 10, 2011.

[14] Ostro et al. 2006; Zanobetti and Schwartz 2011.

[15] O’Neill et al. 2005.

[16] Baja et al. 2010.

[17] Hampel et al. 2012.

[18] Hoffmann et al. 2012.

[19] Dubowsky et al. 2006.

[20] Min et al. 2009; Park et al. 2010.

[21] Brook et al. 2013.

[22] Wagner et al.

[23] Arteriosclerosis, Thrombosis, and Vascular Biology; Rajagopalan 2014.

[24] Brook et al. 2014.

[25] Alshaarawy et al. 2013.

[26] Feng et al. 2014.

[27] Lind et al. 2011.

[28] Airaksinen et al. 2011.

[29] Ibid; Ha et al. 2007; Lee et al. 2012; Uemura et al. 2009.

[30] Arsenescu et al. 2008; Ruzzin et al. 2010.

[31] Hamilton 2002; Grün and Blumberg 2007; Newbold 2010.

[32] Yanagisawa et al.

[33] Valvi et al. 2011.

[34] Melzer et al. 2008.

[35] Yan et al. 2011; Yan et al. 2013; Gao et al. 2013.